THE ROLE OF LEFT ATRIAL COMPLIANCE IN THE DEVELOPMENT OF PULMONARY HYPERTENSION IN PATIENTS WITH PURE MITRAL STENOSIS AND SINUS RHYTHM
Basrah Journal of Surgery,
2012, Volume 18, Issue 1, Pages 26-32
AbstractIn patients with mitral stenosis, there is poor correlation between the severity of mitral stenosis, as measured by the mitral valve area and the magnitude of pulmonary hypertension. We tested the hypothesis that left atrial compliance is a major factor determining the height of pulmonary artery pressure in patients with pure mitral stenosis and sinus rhythm.
The right sided and left atrial trans-septal catheterization data was analyzed in 84 patients (67 females, 17 males) with pure MS and sinus rhythm. Pulmonary artery peak systolic, diastolic and mean pressures were obtained through right sided catheterization. The magnitude of the LA a and v waves and the mean (m) LA pressure were measured directly through trans-septal catheterization. A non-compliant LA was considered to exist if the LA v_m pressure difference equaled to or exceeded 10 mmHg. The mitral valve area was determined by echocardiographic and Doppler methods, as were the LA size, LV systolic and diastolic dimensions, and the LV ejection fraction. Multiple regression analysis was performed to determine the most important factor in the determination of pulmonary artery pressure.
Fifty four patients had PAPs≥50 mmHg, 41 of whom had non- compliant LA. Of the 30 patients with PAPs<50 mmHg, 9 had non compliant LA (P<0.0005).There was no significant difference in the mitral valve area between the two groups with and without severe pulmonary hypertension (0.64±0.18 versus 0.73±0.14 cm2, P=0.13). Analysis of the 30 patients with PAPs<50 mmHg showed significantly higher systolic and mean PA pressure in the 9 patients with non-compliant LA (PAPs 40.55±4.64 vs 35.58±7.46 mmHg, P<0.01; PAPm 30.24±3.56 versus 23.15±5.68 mmHg, P<0.01).
In conclusion, impaired LA compliance contributes at least in part to the development of pulmonary hypertension, and may well be the major mechanism responsible for the development of pulmonary hypertension in patients with pure mitral stenosis and sinus rhythm.
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